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1. The effects of a specific PAF acether antagonist (BN 52063) on the response to isocapnic hyperventilation with dry cold air (ISH study) and exercise (EIA study) were assessed in a single dose and short term treatment study in 10 patients with exercise induced asthma[4].

OBJECTIVE: We compared the incidence of late asthmatic response, the changes in airway responsiveness, the degree of epithelial desquamation, and the activation of eosinophils in the airways after induction of allergen-induced asthma and exercise-induced asthma[19].

Inhaled salbutamol was less effective in protecting against exercise-induced asthma at the end of the treatment period in the patients who had received tablet therapy, but otherwise there was no significant change in beta-receptor function of either airways or lymphocytes[21].

To investigate the possibility that stimulation of neural receptors in the posterior pharynx plays a role in the pathogenesis of exercise-induced asthma, we had 10 asthmatic subjects simulate the hyperpnea of exercise by performing eucapnic hypervenilation in the presence and absence of oropharyngeal anesthesia induced by lidocaine[22].

In particular, they possibly provide novel insights into the molecular mechanisms of exercise-induced bronchoconstriction and suggest that enhanced transcription of ALOX5 and its activating protein together with a present predisposition of the subject critically contribute to exercise-induced asthma[23].

In the cross-sectional study, mirth-triggered asthma was more common: with increasing age (P = 0.02); in those who in the last 3 months had taken more doses of salbutamol (P = 0.005), and who had more wheeze, nocturnal symptoms, and early morning symptoms (P < 0.0005); and in those who reported exercise-induced asthma (P < 0.0005) [31].